Eccrine hidrocystomas * Translucent papules 1-3mm * May have bluish tint * Usually solitary, however, multiple lesion may be seen * Occur on the face * May become more prominent in hot weather * Treatment – excision * Topical atropine or scopolamine

Microcystic adnexal carcinoma (sclerosing sweat duct carcinoma) * Generally a very slow-growing plaque or nodule * Occurs most commonly on the upper lip of women * Perineural infiltration is common and may be extensive * TOC Mohs * No reports of metastases

Proliferating trichilemmal cyst * Large exophytic neoplasms * Almost exclusively confined to scalp and back of neck * May ulcerate * Ass with nevus sebaceous * Metastasis may occur * Most respond to surgical excision

Dermoid cyst * Congenital in origin * Chiefly along lines of cleavage * Result from improper embryologic development * Potential for intracranial communication * CT or MRI scan is required to rule this out prior to BX over cranial cleavage planes * Freely mobile and not attached to the skin

Pilonidal cyst * Midline hairy patch or pit in the sacral region with a sinus orifice in the bottom, or a cyst beneath it * Usually becomes symptomatic during adolescence * Opening cyst widely, debriding it, and packing it with silver nitrate crystals * More advanced surgical intervention may be required * SCC has been reported to arise from chronic inflammatory pilonidal disease

* Pearl: General rule of thumb is to shave a tumor and punch a rash. * Pitfall: A shave biopsy of a deep melanoma destroys the prognosis/Breslow’s thickness. Result: Now you must assume the worst and put the patient through extensive surgeries and chemotherapy. Moral: Fully excise or refer all suspected melanomas.

Pearl #2 * Pearl: Know where your biopsy is going. Always specify “must be diagnosed by a dermatopathologist”. * Pitfall: If you do not specify as above it will go to a general pathologist. They may give you less than ideal diagnostic information or even miss the diagnosis. Your patient will not be impressed.

Pearl #4 * Pearl: When the patient asks “what do you think it (the lesion) is?”, the correct answer is “If I knew that I wouldn’t have to do the biopsy”. * Pitfall: Never attempt to reassure the patient by saying the lesion is “probably going to be nothing at all”, they’ll wonder why you’re putting them through all of this.

Local Anesthesia * “Doc, will this hurt?” * “I’m not sure, they’ve only let me try this on animals so far” * “No, it shouldn’t hurt me a bit” * “More than a tickle but less than paying taxes” * Pearl: fears of epinephrine induced necrosis at distal sites (nose, ears, penis, toes, fingertips) are largely unfounded. * Pitfalls: patients with severe peripheral vascular disease, diabetic angiopathy and Raynaud’s phenomenon may be exceptions to the rule.

Pearl #5 * Local Anesthesia: * Pearl: INJECT SLOWLY and your patients will love you forever. Decreases pain more than warming or adding bicarbonate. * Pitfall: ALWAYS make sure they are lying down, especially the patient who “talks tough”.

Pearl #6 * Local Anesthesia * Pearl: It is OK to give Xylocaine to patients who had allergic reactions to Novocaine at the dentist’s office, Lidocaine is an Amide and Novocaine is an Ester. * Pitfall: They may not know which medication they reacted to: use Bacteriostatic NS when in doubt.

Pearl #7 * Local Anesthesia * Pearl: For pediatric patients, let them sit in the lobby with ELA-Max or EMLA covered with Saran Wrap for 30 minutes. * Pitfall: The above may fail. At this point either refer or insert earplugs and proceed. Remember: very few pediatric rashes will require biopsy for diagnosis.

Pearl #8 * Pearl: Insert needle at a 30 degree angle and slowly retract the needle as you inject the anesthetic. When the tissue blanches you are at the right level. * Pitfall: If you see a linear trail of blanched skin radiating from the injection site you are probably in a vessel.

Pearl #9 * Regarding Coumadin. * Pearl: Do not take patients off Coumadin to perform a small dermatologic procedure such as biopsy, excision or Moh’s surgery. * Pitfalls: Depend on the reason why they are on Coumadin in the first place. Also problematic if you do not have tools for hemostasis.

Shave Biopsy - skin tensionShave Biopsy - flush with surface * Endpoint is “pinpoint bleeding” * Indicates you are at the level of the papillary dermis * This is where scarring begins and patient satisfaction decreases. * Pearl: Stay superficial and you can achieve minimal scarring. * Pink atrophic area has a full year to heal. * Pitfalls: Skin of upper chest and back scars no matter what. Same with Keloid prone pts.

Excisional Biopsy * Pearl: If you suspect melanoma excisional biopsy DOWN TO FAT. * Pitfalls: Punch biopsy, while deep enough is NOT representative of the entire lesion. Shave too shallow, prognosis destroyed. * Pitfalls: Excision takes more time, reimbursement same, but medicolegally still a bargain because it is the standard of care. * Using a Sharpie felt tip pen mark a circle around lesion with about 1-2 mm margins around clinically apparent lesion. * Ellipse should be 3 times longer than circle around lesion. * Pearl: Try to postion the final suture line within existing wrinkle lines / least tension. * Whether lesion is malignant or not, your patient will never forget their scar. * Sterile procedure! * H2O2 and Betadine * Pearl: Try not to apply the above too aggressively or to get excess Xylocaine on your ellipse drawing * Pitfall: ink will rinse away, now you’re lost!

Polymorphic Eruption of Pregnancy * Pruritic inflammatory dermatoses of pregnancy occur in 1 of every 120 to 240 * Treatment and prognosis is similar in subtypes

Pruritic Urticarial Papules and Plaques of Pregnancy (PUPP) * First reported in 1979 * Erythematous papules and plaques that begin as 1-2 mm lesions within the abdominal striae * Spread over the course of a few days to involve the abdomen, buttocks, thighs * Upper chest, face, and mucous membranes spared

PUPPP * Lesions coalesce to form urticarial plaques * Intense pruritis is characteristic * Primigravidas 75% of the time, usually does not recur with subsequent pregnancies * Begins late in third trimester and resolves with delivery * May be associated with increase weight gain * Histology: perivascular infiltrate in upper and mid dermis, epidermis normal * Tx: topical or oral steroids

Dermatitis Herpetiformis * Eruption usually symmetrical * Scalp, nuchal area, posterior axillary folds, sacral region, buttocks, knees, forearms * Pruriginous papules are a common feature * Vesicles are more common than bullae; however all types of these lesions may be present in one patient * Course of the disease is generally lifelong, with prolonged remissions being rare

Dermatitis Herpetiformis * Very few patients with DH ever have diarrhea although DH is associated with Gluten-sensitive-enteropathy (GSE) * 87% of pts with DH and IgA deposits in the skin are HLA-B8 positive (like GSE) * Gluten is a protein found in cereals except for rice, oats, and corn * IgA antibodies are formed in the jejunum, may deposit in the skin * Associated with; Thyroid disorders, small bowel lymphoma, non-Hodgkins lymphoma * 70% of pts have abnormalities of the jejunal mucosa * Gluten-free diet decreases Dapsone dose requirements after 3-4 months * Ddx: pemphigoid, EM, scabies, contact dermatitis, atopic dermatitis, eczema, insect bites, pruigo nodularis * IgA in a granular pattern in the dermal papillae in normal skin is specific and pathognomonic for DH * IgA deposits may be focal, so multiple biopsies may be needed. * Deposits of the antibody are more often seen in previously involved skin or normal appearing skin adjacent to involved skin * Equal male:female * Onset between 20 to 40 years * Tx: Dapsone 50-300mg daily (hemolytic anemia, methemoglobinemia, check G6PD prior to tx) monitor Hct,WBCs, LFTs * Tx: Sulfapyridine 0.5g QID to 2-4g/day * Gluten-free diet will decrease need for meds or allow pt to go off them Celiac Society

Linear IgA Bullous Dermatosis Adult Form * Acquired autoimmune blistering disease * Clinical pattern similar to dermatitis herpetiformis, or with vesicles and bullae in a bullous pemphigoid-like appearance * 50% mucous membrane involvement * Oral and conjunctival lesions may be scarring * No association with enteropathy or with HLA-B8 * Tends to remit over several years

Linear IgA Bullous Dermatosis Adult Form * Linear IgA dermatosis can occur as a drug-induced disease: * Self-limited, less mucosal involvement, usually does not have circulating autoantibody * IgA is usually deposited in the subbasal lamina area * Vanco, Lithium, amiodarone, captopril, PCN, lasix, dilantin, and others * Histo: papillary dermal microabscess with neutrophils, subepidermal bullae may be seen with neutrophils and eosinophils * Direct IF: homogeneous linear deposition of IgA is present at the BMZ * Indirect IF: few will have circulating IgA autoantibody with anti-BMZ specificity * Tx: Dapsone, topical steroids

Nutritional Diseases * Caused by insufficiency or excess of dietary essentials * Common in underdeveloped countries, infants and children * Often pts have features of several disorders if diet is generally restricted * Alcoholism is the main cause in developed countries * Postoperative pts, psychiatric pts (anorexia nervosa, bulimia), surgical or inflammatory bowel dysfunction, Crohn’s

Hypovitaminosis A (Phrynoderma) * Vitamin A: fat soluble found in milk, fish oil, liver, eggs, and as carotenoids in plants * Common in children in developing world * Developed countries found in diseases of fat malabsorption; Crohn’s, celiac, cystic fibrosis, cholestatic liver disease * Vitamin A required for keratinization of mucosal surfaces * Abnormal keratinization leads to increased mortality from inflammatory disease of the gut and lung ie; diarrhea and pneumonia * Phrynoderma or “toadskin” resembles keratosis pilaris. * Keratotic papules over extremities and shoulders arising from pilosebaceous follicles * Eruption begins on thighs or upper arms. Spreads to shoulders, abdomen, back, and buttocks, face and neck * Skin displays dryness and scaling

Hypovitaminosis A Ocular Findings * Major cause of blindness in children in the developing world! * Earliest finding is delayed adaptation to the dark (nyctalopia) * Night blindness, xeropthalmia, xerosis corneae, keratomalacia * Bitot’s Spots; circumscribed areas of xerosis of the conjuctiva lateral to the cornea

* Skin findings similar to side effects of Retinoid therapy. Children are at greater risk. * Loss of hair and coarseness, loss of eyebrows, exfoliation and pigmentation of skin, clubbing, hepatosplenomegaly, anemia, increased LFTs, pseudotumor cerebri with papilledema

Hypervitaminosis A Adults * Early signs are dryness of the lips and anorexia. Followed by bone and joint pains, follicular hyperkeratosis, branny desquamation of the skin, loss of scalp hair and eyebrows, dystrophy of the nails. * Fatigue, myalgia, depression, anorexia, liver disease * Birth defects with excess Vit A in pregnancy

Niacin Deficiency Pellagra * Nicotinic acid, vitamin B3, niacin or its precursor tryptophan is associated with a diet entirely composed of corn, millet or sorghum * Other vitamin defficiencies or malnutrition coexist * Most cases are alcoholics in developed countries

Ehlers-Danlos syndromes * A group of genetically distinct disorders characterized by excessive stretchability and fragility of the skin * Tendency toward easy scar formation, calcification of the skin to produce, pseudotumors, and hyperextensibility of the joints

Secondary cutaneous amyloidosis * Following PUVA therapy and in benign and malignant cutaneous neoplasms, deposits of amyloid may be found * Most frequently associated neoplasms are NMSC and SKs * In all cases, this is keratin-derived amyloid

PORPHYRIAS * Porphyrinogens are the building blocks of hemoproteins * Produced primarily in the liver, bone marrow and erythrocytes * Each form is associated with a deficiency in the metabolic pathway of heme synthesis * Absorption of UV radiation in the Soret band (400-410 nm) by the increased porphyrins leads to photosensitivity * Activated porphyrins form reactive oxygen species that causes tissue damage

Variegate porphyria VP * AD * Decreased activity of protoporphyrinogen oxidase * Majority of relatives have silent VP * Characterized by skin lesions of PCT and the GI and neurologic disease of AIP * Suspect VP when finding indicate both PCT and AIP, esp. with history of South African ancestry * Fecal coproporphyrins and protoporphyrins are always elevated * During attacks, urine porphobilinogen and ALA are elevated * Urinary coproporphyrins are increased over uroporphyrins * A finding in the plasma of “X porphyrin,” fluorescence at 626 nm is characteristic and distinguishes this form from others * Symptomatic treatment as for PCT and AIP

* Report of seven infants exposed to 380 to 700 nm blue lights, for the treatment of indirect hyperbilirubinemia, who developed marked purpura on the exposed skin * All infants had received transfusions * Elevated plasma coproporphyrins and protoporphyrins were found in 4 * Pathogenesis is unknown

Hypersensitive Carotid Sinus Syndrome • Syncope or presyncope due to an exaggerated response to carotid sinus stimulation• Defined as asystole greater than 3 sec due to sinus arrest or AVHB, an abrupt reduction of BP, or both

Neurally Mediated Syncope * 10-40% of patients with syncope * Triggering of a neural reflex * Use of pacemakers is controversial since often bradycardia occurs after hypotension

Indications for ICDs * Cardiac arrest due to VT/VF not due to a transient or reversible cause * Spontaneous sustained VT * Syncope with hemodynamically significant sustained VT or VF * NSVT with CAD, previous MI, LV dysfunction and inducible VF or VT not suppressed by a class 1 antidysrhythmic

Atrial arrhythmiaPremature contractions * The term “premature contractions” are used to describe non sinus beats. * Common arrhythmia * The morbidity rate is 3-5%Atrial premature contractions (APCs) * APCs arising from somewhere in either the left or the right atrium. * Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemia * Symptoms: many patients have no symptom, some have palpitation, chest incomfortable. * Therapy: Needn’t therapy in the patients without heart disease. Can be treated with ß-blocker, propafenone, moricizine or verapamil.

Sinus arrhythmia * Usually respiratory--Increase in heart rate during inspiration * Exaggerated in children, young adults and athletes—decreases with age * Usually asymptomatic, no treatment or referral * Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicity * Referral may be necessary if not clearly respiratory, history of heart disease

Sick Sinus Syndrome * All result in bradycardia * Sinus bradycardia (rate of ~43 bpm) with a sinus pause * Often result of tachy-brady syndrome: where a burst of atrial tachycardia (such as afib) is then followed by a long, symptomatic sinus pause/arrest, with no breakthrough junctional rhythm.

Atrial fibrillation--management * Rhythm vs Rate control—if onset is within last 24-48 hours, may be able to arrange cardioversion—use heparin around procedure * Need TEE if valvular disease (high risk of thrombus) * If unable to definitely conclude onset in last 24-48 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and warfarin for 4-12 weeks after

Atrial Fibrillation * Cardioversion: synchronized (w/QRS) delivery of current to heart; depolarizes tissue in a reentrant circuit; afib involves more cardiac tissue, but cardiovert * Defibrillation: non-synchronized delivery of current

Atrial fibrillation--management * Rate control with chronic anticoagulation is recommended for first line approach for majority of patients; overall Afib is a stable rhythm * Beta-blockers (atenolol and metoprolol) or calcium channel blockers (verapamil or diltiazem) recommended. Digoxin not recommended for rate control * Anticoagulation: LMWH and then warfarin; can use aspirin for anticoagulation if CI to warfarin, not as effective

* Progressive PR longation, with eventual non-conduction of a p wave * May be in 2:1 or 3:1Wenckebach, Mobitz type I * Usually asymptomatic, but with accompanying bradycardia can cause angina, syncope esp in elderly—will need pacing if sxs * Also can be caused by drugs that slow conduction (BB, CCB, dig) * 2-10% long distance runners * Correct if reversible cause, avoid meds that block conduction

* Alternating patterns of bradycardia and tachycardia * Often there is a long pause (asystole) between heartbeats, especially after an episode of tachycardia * Tachycardia: PSVT, atrial fibrillation, atrial flutter

causes

* Most cases are idiopathic * Intrinsic causes * Extrinsic causes * Cardiac surgery, especially to the atria, is a common cause of sick sinus syndrome in children.

Clinical manifestations

* Many people with sick sinus syndrome have no symptoms * Symptoms are related to the decresed cardiac output that occurs with the bradyarrythmias or tachyarrythmias * Fainting , Fatigue , Shortness of breath, or dyspnea, Chest pains , Confusion , Palpitations * Bradycardia-tachycardia syndrome: peripheral thromboembolism and stroke

Treatment

* If the disorder is asymptomatic (without symptoms), no treatment is necessary * Bradycardia-tachycardia syndrome * Associated tachycardia may be treated with medications after the person is protected from symptomatic bradycardia by a pacemaker. * Warfarin has been shown to decrease the number of strokes and embolic events

Mechanisms of ArrhythmogenesisSinus Arrhythmia EKG Characteristics: Presence of sinus P waves Variation of the PP interval which cannot be q attributed to either SA nodal block or PACs

When the variations in PP interval occur in phase with respiration, this is considered to be a normal variant. When they are unrelated to respiration, they may be caused by the same etiologies leading to sinus bradycardia.

Sick Sinus Syndrome * Characterized by a collection of symptoms and ECG findings due to chronic dysfunction of the sinoatrial (SA) node: o Chronic and severe sinus bradycardia o Sinus pauses o Sinus arrhythmia o Complete sinus arrest o Progressive development of atrial arrhythmias (a-flutter, a-fib, atrial tachycardia) * Patients are usually elderly and present with lightheadedness and/or syncope, but it can also manifest as angina, dyspnea, and palpitations.

* About 50% of people with SSS also display some degree of dysfunction of the AV nodeSinus bradycardia (rate of ~43 bpm) with a sinus pause

Etiologies of Sick Sinus Syndrome Familial SSS (due to mutations in SCN5A)Infiltrative diseasesPericarditisLyme diseaseHypothyroidismRheumatic fever Sinus node firbosis Atherosclerosis of the SA arteryCongenital heart diseaseExcessive vagal toneDrugsTachycardia-Bradycardia Syndrome * Common variant of sick sinus syndrome severe bradycardia alternates with paroxysmal tachycardias, most often atrial fibrillation. * There is usually a prolonged pause in the cardiac rhythm following cessation of the tachyarrhythmia.Tachycardia-Bradycardia Syndrome Abrupt termination of atrial flutter with variable AV block, followed by sinus arrest with a junctional escape beat.

Multifocal Atrial Tachycardia Bigeminal Rhythms * Arrhythmias in which each normal sinus beat is followed by a premature contraction (PAC, PJC, or PVC). * Results in a couplet rhythm which can be detected by pulse or auscultation. * Generally benignAtrial BigeminyVentricular BigeminyPreexcitation ECG Characteristics of WPW: 1. Short PR interval 2. QRS prolongation 3. Delta wave Preexcitation is a condition characterized by an accessory pathway of conduction, which allows the heart to depolarize in an atypical sequence.The most common form of preexcitation is called Wolfe-Parkinson-White (WPW) syndrome, in which a direct atrioventricular connection allows the ventricles to begin depolarization while the standard action potential is still traveling through the AV node.

AV Reentrant Tachycardia (AVRT) In patients with WPW, a reentrant rhythm can be generated where the AV node serves as one arm of the reentrant circuit, and the accessory pathway as the other.

Types of AVRT * Orthodromic AVRT (More common) – Narrow complex tachycardia in which the wave of depolarization travels down the AV node and retrograde up the accessory pathway. * Antidromic AVRT (Less common) – Wide complex tachycardia in which the wave of depolarization travels down the accessory pathway and retrograde up the AV node.

Mechanism of orthodromic AVRTMechanism of antidromic AVRTWhat is this arrhythmia? Antidromic AVRTClassification Scheme for Arrhythmias

There are 26 bones in the foot; all but five are involved in at least two joints. * Hind foot * Midfoot * Forefoot * foot biomechanics1

Subtalar joint: where the talus rests on and articulates with the calcaneus. This is a synovial joint with a weak capsule supported by medial, lateral, posterior & interosseous talocalcaneal ligaments.

* The interosseous talocalcaneal ligament (very strong) lies in the tarsal sinus (separates the anterior & posterior talocalcaneal joints). * Anatomical subtalar joint- functionally a single synovial joint between the slightly concave articular surface of the talus and the convex posterior articular surface of the calcaneus.

* The main movement at these joints are foot eversion & inversion, eversion is augmented by extension of the toes (especially the lateral toes), inversion is augmented by toe flexion especially the 1st &2nd toes.

Transverse tarsal joints – a compound joint1. Talonavicular part of the talocalcanealnavicular joint

2. Calcaneocuboid joint

* These 2 separate joints are aligned transversely. At this joint the forefoot & midfoot rotate as a unit on the hind foot around an AP axis. This augments inversion/eversion of the foot. * Anatomical amputations of the foot are made through this joint.

1. Intertarsal joints: These bones are so tightly opposed by ligaments that little movement occurs between them

All the joints proximal to the metatarsalphalangeal joints are united by dorsal & plantar ligaments.

All the bones of the metatarsals and interphalangeal joints are united by lateral & medial collateral ligaments.

Major ligaments of the Plantar foot Plantar calcaneonavicular (Spring) ligament

* Fills a wedge shaped gap between the talar shelf & inferior margin of the posterior articular surface of the navicular. This ligament supports the head of the talus and plays an important role in the transfer of weight from the talus & maintaining the longitudinal arch.

Long Plantar Ligament * Traverses from the plantar surface of the calcaneus to the groove on the cuboid. Some fibers extend to the base of the metatarsals (forming a tunnel for the tendon of the fibularis longus. This ligament is important in maintaining the longitudinal arch.

Plantar calcaneocuboid (short plantar) ligament: * Located deep to the long plantar ligament, it runs from the anterior part of the inferior surface calcaneus to the inferior surface of the cuboid. It is located on a plane between the plantar calcaneonavicular (spring) ligament and the long plantar ligament. It is also involved in maintenance of the longitudinal arch.

Arches of the Foot * The ligamentous bony arrangement of the foot allows considerable flexibility/deformation with weight bearing contact. The arches distribute the weight of the foot (pedal platform) acting both as shock absorbers & spring boards during ambulation of all types. * Weight distribution is between the calcaneus and sesamoid bones at the 1st metatarsal and head of the 2nd metatarsal; weight is shared laterally with the heads of metatarsals 3-5. Elastic arches between weight bearing points compress with loading and recoil with unloading. * Lateral Longitudinal arch * Medial Longitudinal arch * Transverse Arch

All three work as a unit in weight bearing

* Medial Longitudinal Arch higher and more prominent than the lateral arch. * Consists of the calcaneus, talus, navicular, 3 cuneiforms and 3 metatarsals * Talar head is the keystone of the medial longitudinal arch * The medial arch is supported by the Tibialis anterior ligament as it attaches to the 1st metatarsal and medial cuneiform. Also the tib posterior & FHL. * The tendon of the fibularis longus passes from lateral to medial and also supports the medial longitudinal arch. * Lateral Longitudinal Arch is much flatter and consists of the calcaneus, cuboid & lateral metatarsals. * The medial arch is involved in weight bearing while the lateral arch is involved in balance * Transverse arch: cuboid, cuneiforms and bases of the metatarsals. This forms the medial & lateral parts of the longitudinal arches which serve as pillars fro the transverse arch. * The tendon of the fibularis longus & tibialis posterior crossing the sole of the foot obliquely help maintain the curve of the transverse arch. * The Arches of the foot are maintained by both passive & dynamic supports.

Passive factors1. Shape of the united bones (especially the transverse arch).

Pes Planis (flat feet) Prior to 3 years of age it is normal to have flat feet due to a fat pad. After the age of 3 this fat pad disappears.

Pes planis can be classified as:

* Flexible: the arch is normal when unloaded however with loading the arch is lost. this is the most common type. It is due to inadequate passive arch support (weak, loose ligaments). * Rigid type, the arch is absent regardless of loading, this may be due to a congenital deformity.

* Acquired “fallen arches” is due to a tibialis posterior dysfunction due to trauma, denervation and/or degeneration. The plantar calcaneal ligament fails allowing the head of the talus to rotate inferomedially creating a prominence on the medial aspect of the mid-hind foot junction. This is often referred to as over pronation.

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